The cardiopulmonary baroreflex responds to an increase in central venous pressure (CVP) by decreasing total peripheral resistance and increasing heart rate (HR) in dogs. However, the direction of ventricular contractility change is not well understood. The aim was to elucidate the cardiopulmonary baroreflex control of ventricular contractility during normal physiological conditions via a mathematical analysis. Spontaneous beat-to-beat fluctuations in maximal ventricular elastance (E-max), which is perhaps the best available index of ventricular contractility, CVP, arterial blood pressure (ABP), and HR were measured from awake dogs at rest before and after beta-adrenergic receptor blockade. An autoregressive exogenous input model was employed to jointly identify the three causal transfer functions relating beat-to-beat fluctuations in CVP to E-max (CVP -> E-max), which characterizes the cardiopulmonary baroreflex control of ventricular contractility, ABP to E-max, which characterizes the arterial baroreflex control of ventricular contractility, and HR to E-max, which characterizes the force-frequency relation. The CVP -> E-max transfer function showed a static gain of 0.037 +/- 0.010 ml(-1) (different from zero; P < 0.05) and an overall time constant of 3.2 +/- 1.2 s. Hence, E-max would increase and reach steady state in similar to 16 s in response to a step increase in CVP, without any change to ABP or HR, due to the cardiopulmonary baroreflex. Following beta-adrenergic receptor blockade, the CVP -> E-max transfer function showed a static gain of 0.0007 +/- 0.0113 ml(-1) (different from control; P < 0.10). Hence, E-max would change little in steady state in response to a step increase in CVP. Stimulation of the cardiopulmonary baroreflex increases ventricular contractility through beta-adrenergic receptor system mediation.
